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Your search keyword '"Clair, Mark J."' showing total 25 results
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25 results on '"Clair, Mark J."'

1. Advanced glycation end products are elevated in estrogen receptor-positive breast cancer patients, alter response to therapy, and can be targeted by lifestyle intervention

Author

Walter, Katherine R., Ford, Marvella E., Gregoski, Mathew J., Kramer, Rita M., Knight, Kendrea D., Spruill, Laura, Nogueira, Lourdes M., Krisanits, Bradley A., Phan, Van, La Rue, Amanda C., Lilly, Michael B., Ambs, Stefan, Chan, King, Turner, Tonya F., Varner, Heidi, Singh, Shweta, Uribarri, Jaime, Garrett-Mayer, Elizabeth, Armeson, Kent E., Hilton, Ebony J., Clair, Mark J., Taylor, Marian H., Abbott, Andrea M., Findlay, Victoria J., Peterson, Lindsay L., Magwood, Gayenell, and Turner, David P.

Published
2019
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3. Myocardial matrix metalloproteinase activity and abundance with congestive heart failure

Author

Coker, Mytsi L., Thomas, Chadwick V., Clair, Mark J., Hendrick, Jennifer W., Krombach, R. Stephen, Galis, Zorina S., and Spinale, Francis G.

Subjects
Congestive heart failure -- Physiological aspects, Metalloenzymes -- Physiological aspects, Heart ventricle, Left -- Physiological aspects, Extracellular matrix -- Physiological aspects, Biological sciences
Abstract

The relative abundance of specific matrix metalloproteinases (MMPs) was investigated during congestive heart failure (CHF). With pacing CHF, left ventricular (LV) myocardial zymographic activity for the substrate gelatin increased by 119% and for the substrate collagen III by 153% over controls. Caseinolytic activity also increased with pacing CHF by 139% over controls. Thus, LV myocardial MMP activity and abundance increased with pacing-induced CHF.

Published
1998

7. Advanced glycation end products are elevated in estrogen receptor-positive breast cancer patients, alter response to therapy, and can be targeted by lifestyle intervention

Author

Walter, Katherine R., primary, Ford, Marvella E., additional, Gregoski, Mathew J., additional, Kramer, Rita M., additional, Knight, Kendrea D., additional, Spruill, Laura, additional, Nogueira, Lourdes M., additional, Krisanits, Bradley A., additional, Phan, Van, additional, La Rue, Amanda C., additional, Lilly, Michael B., additional, Ambs, Stefan, additional, Chan, King, additional, Turner, Tonya F., additional, Varner, Heidi, additional, Singh, Shweta, additional, Uribarri, Jaime, additional, Garrett-Mayer, Elizabeth, additional, Armeson, Kent E., additional, Hilton, Ebony J., additional, Clair, Mark J., additional, Taylor, Marian H., additional, Abbott, Andrea M., additional, Findlay, Victoria J., additional, Peterson, Lindsay L., additional, Magwood, Gayenell, additional, and Turner, David P., additional

Published
2018
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11. Effects of Growth Hormone Supplementation on Left Ventricular Morphology and Myocyte Function With the Development of Congestive Heart Failure

Author

Houck, Ward V., primary, Pan, Lydia C., additional, Kribbs, Scott B., additional, Clair, Mark J., additional, McDaniel, George M., additional, Krombach, R. Stephen, additional, Merritt, William M., additional, Pirie, Christine, additional, Iannini, Julie P., additional, Mukherjee, Rupak, additional, and Spinale, Francis G., additional

Published
1999
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13. AT1 angiotensin II receptor inhibition in pacinginduced heart failure: Effects on left ventricular performance and regional blood flow patterns

Author

Clair, Mark J., primary, Krombach, R.Stephen, additional, Hendrick, Jennifer W., additional, Houck, Ward V., additional, Hebbar, Latha, additional, Kribbs, Scott B., additional, Rios, Gloria, additional, Whitebread, Steve, additional, Mukherjee, Rupak, additional, de Gasparo, Marc, additional, and Spinale, Francis G., additional

Published
1998
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15. Chronic Amlodipine Treatment During the Development of Heart Failure

Author

Spinale, Francis G., primary, Mukherjee, Rupak, additional, Krombach, R. Stephen, additional, Clair, Mark J., additional, Hendrick, Jennifer W., additional, Houck, Ward V., additional, Hebbar, Latha, additional, Kribbs, Scott B., additional, Zellner, James L., additional, and Dodd, Michael G., additional

Published
1998
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20. Angiotensin converting enzyme inhibition, AT1 receptor inhibition, and combination therapy with pacing induced heart failure: effects on left ventricular performance and regional blood flow patterns.

Author

Krombach, R.Stephen, Clair, Mark J, Hendrick, Jennifer W, Houck, Ward V, Zellner, James L, Kribbs, Scott B, Whitebread, Steve, Mukherjee, Rupak, de Gasparo, Marc, and Spinale, Francis G

Abstract

Background: AT1 receptor activation has been demonstrated to cause increased vascular resistance properties which may be of particular importance in the setting of congestive heart failure (CHF). The overall goal of this study was to examine the effects of ACE inhibition (ACEI) alone, AT1 receptor blockade alone and combined ACEI and AT1 receptor blockade on LV pump function, systemic hemodynamics and regional blood flow patterns in the normal state and with the development of pacing induced CHF, both at rest and with treadmill induced exercise. Methods and results: Pigs (25 kg) were instrumented in order to measure cardiac output (CO), systemic (SVR) and pulmonary vascular (PVR) resistance, neurohormonal system activity, and myocardial blood flow distribution in the conscious state and assigned to one of 4 groups: (1) rapid atrial pacing (240 bpm) for 3 weeks (n=7); (2) ACEI (benazeprilat, 3.75 mg/day) and pacing (n=7); (3) AT1 receptor blockade (valsartan, 60 mg/day) and rapid pacing (n=7); and (4) ACEI and AT1 receptor blockade (benazeprilat/valsartan, 1/60 mg/day, respectively) and pacing (n=7). Measurements were obtained at rest and with treadmill exercise (15°, 3 miles/h; 10 min) in the normal control state and after the completion of the treatment protocols. With rapid pacing, CO was reduced at rest and with exercise compared to controls. ACEI or AT1 blockade normalized CO at rest, but remained lower than control values with exercise. Combination therapy normalized CO both at rest and with exercise. Resting SVR in the CHF group was higher than controls and SVR fell to a similar degree with exercise; all treatment groups reduced resting SVR. With exercise, SVR was reduced from rapid pacing values in the ACEI and combination therapy groups. PVR increased by over 4-fold in the rapid pacing group both at rest and with exercise, and was reduced in all treatment groups. In the combination therapy group, PVR was similar to control values with exercise. Plasma catecholamines and endothelin levels were increased by over 3-fold with chronic rapid pacing, and were reduced in all treatment groups. In the combination therapy group, the relative increase in catecholamines and endothelin with exercise were significantly blunted when compared to rapid pacing only values. LV myocardial blood flow at rest was reduced in the rapid pacing only and monotherapy groups, but was normalized with combination therapy. Conclusion: These findings suggest that with developing CHF, combined ACE inhibition and AT1 receptor blockade improved vascular resistive properties and regional blood flow distribution to a greater degree than that of either treatment alone. Thus, combined ACEI and AT1 receptor blockade may provide unique benefits in the setting of CHF. [ABSTRACT FROM PUBLISHER]

Published
1998
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